muscles Flashcards
what muscls are voluntary
skeletal
which muscles are involuntary
smooth and cardiac
features of skeletal muscles
elongated cells
multiple nuclei
visible striations
cardiac muscle features
branched cels
single or double nuclei
visible triations
smooth muscle features
spindle cells
single central nuclei
no striations
how does endothelum-dependent vasular relaxation work?
vessel walls are innervated by nerves parasympathetic released bradykinin/acetylcholine Ca flows into endothelial cell activates nitrix oxide synthase diffuses into the cell causes activation to make GTP and GMP calcium is taken back up cell relaxes
briefly describe how smooth muscle relaxes
Ca in activates bigger store activates calmodulin binds to it phosphryates myosin chain kinase kinase phosphoryates myosin head power stroke
briefly describe smooth mucle relxation
calcium removed from cytosol
ATP depenent pump
ATPase decrease
no muscle tension
how domyocardial cells work
elecrical impulse sprads through intercollated disks
the pulse triggers electrogenic pups to open allowing Na in
negative potential to positive
influx of Na and Ca
plateau short
what is excitation contraction coupling
Ca in through L type channels in T tubules
calcium induced calcium receptors open using RYR
Ca interacts with tropnin revealing binding sites
ca reabsorbed by SERCA and pumups
unbinds from troponin and sarcomere goes back to rest
what is SERCA
sarco-endopasmic reticulum Calcium ATPase
define epimysium
connective tissue around muscle
define fasciles
bundles of muscle fibres within the epimysium
define perimysium
connective tissue around fascicles
define endomysium
indivual myofibre muscle cells surrounded by connective tissue
define sarcolemma
plasam membrane of skeletal muscle
define T-tubule
invagination allowing electrical impulses deep into the muscules
define sarcoplsmic reticulum SR
surronds each myofibril ear the tubule
key calcium store
define triad
where the sarcoplasmic reticulum meets the T tubule
define the A band
dark
thick filaments only
define the I band
light
thin filaments only
length increases during contraction
define the Z line
intersects the I band
filaments attach here
separates adjacent sarcomeres
adheres everything. transmits the force from one sarcomere to another
define the H zone
length decreases during contraction
define the M line
middle of the A band
thick filaments attach to here
what is a motor unit?
a motor neuron and all the myofibrils it innervates
how can motos unit size vary?
for fine control there are smaller motor units
larger muscles however use large motor units for more force in movement
what is the presynaptic terminal?
the nerve fibre
vesicles containing neurotranmitters are found here to be releseased
how wide is the synpatic celft?
20-30nm wide
what neurotransitter is used at the NMJ
acetylcholine Ach
what is a voltage gated calcium channels
found on the presynaptic membrane of the neurone
when action potentaisl go across the membrane thee channels open allowing calcium into the syanptic space and to the nerve terminal
how do vesicles release theor contents across the cleft?
exocytosis
what is an acetylcholine receptor made up of?
2 alpha subunits
1 beta
1 gamma
1 delta
what opens Ach gates?
2 Ach molecules attaching to the 2 alpha subunits
describe the process of action potentials moving from the nerve to the muscles
- arrival of action potential at the synapse causes a Ca influx due to opening of voltage gated channels
- causes Ach vesicles to move to presynpase membrane and be released via excytosis diffusing across the cleft
- they bind Ach receptors on muscle membrane
depolarization spreads out to other parts of the muscle
what is EPP/ what causes it
end plate potential
is made when the muscle depolarises
influx of Na in the muscle leads to the initiation of it
what is the end plate potential
creates a local positive potential as sodium moves into the muscle fibre
the end plate creates an action potential that can then spread along the muscle membrane causing contraction
what breaks down Ach
acetylcholinersterase into Acetyl CoA and choline
these are then taken back up by the presynaptic terminal where its synthesised back into the neurotransmitter
what is uscle fatigue
when the muscle is overstimulated and run out of vesicles
signals are then inhibited
define high safety factor
each impulse reaching the NMJ is 3 times as much end plate potential needed to stimulate the fibre
therefore teh NMJ is said to have this high safety factor
how does muscle fatigue occur?
too much stimulation of the uscle too fast leading to a reduced number of vesicles available
impulses fail to be passed onto the muscle
what does a drug blocking the release of Ach do?
it inactivates the muscles around because there is no releace of the neurotransmitter
muscles cannot contract anymore
example of a drug that blocks the release of Ach
botulinum
it fuses with the vesicles preventing exocytosis
how do drugs stimulate muscle through imitation of ach activity?
cause depolarisation of muscle fibres
except they dont get broken back down again so their action can persist for minutes to hours
they cause localised areas of depolarization of fibre at end plate
constant stage of muscle spasm
examples of drugs immitating Ach activity
methacholine and nicotine
how can some drugs inactivate acetlycholinesterase
combine with it in the synaptic cleft so it cannot work
therfore with each impulse, additional Ach accumulates and stimulates the fibre repetitively
what is the issue with drugs that inactivate acetylcholinesterase
causes muscle spasm
if in the larynx it can cause spasm here leading to smothering and death
what is an example of a drug inactivating Ach-ase
diisopropyl flurophosphte
effective lethal poison with military potential
is effective for weeks
used as a ‘nerve gas poison’
examples of drugs that block transmission at junctions
curariform drugs
what do curariform drugs do
prevent the passage of impulses from the nerve ending into the muscles
they compete for receptor sits, when the drug binds Ach cannot
theurapeutic uses of drugs which block transmission at jucntions
artifical respiration to control convulsions in tetanus
during surgery when compete muscle relaxation is needed
describe excitation- contraction coupling
Ach released and NMJ
NA enters through Ach receptors initiating an action potential
potential in T tubules alters conformation of DHP receptor
DHP receptor open Ca channels
Ca binds t troponin allowing actin-myosin binding
myosin heads do power stroke
muscle tension
what cant myosin be cleaved into?
LMM
HMM
light and heavy mereomyosin
what allows myosin to reach bindng sites of actin?
a hinge on the LMM and HMM parts
it can flex here
what are thin filaments made of
actin
tropnin
tropmyosin
what covers the binding sites on actin for myosin?
troponin
what is MBS
myosin binding sites on actin
how is actin made
its a chain of gamma actin monomers forming a polymer chain of F actin
this then forms a double helix strand where two strand wrap around each other
what causes the cessation of contraction in muscles
muscle will keep contracting as long as it has ATP
once the enrgy is depleated the muscle has to stop slowly
contraction is terminated by Ca being removed
how is Ca remove?
Ca pump called SERCA
what si SERCA
Ca pump that goes against concentration gradients so required energy/ ATP
what happens during rigor motis
calcium cannot be taken up from the cytosol space and there is no ATpase actiity
so there are high amounts of it
meaning actin cant dissociate from myosin
contraction cycle stuck
relaxation cannot take place
state of continuous contraction
when is ATP used in muscle contraction
- generating high emerg stage from myosin
- disconecting mysin from actin
- pumping Ca from cytosol back to SR
where can the muscles ge ATp from
glycoloysis
ceratin phosphate
krebs cycle
what is creatine hosphate
a means of storing energy
found in high energy using tissues suchas brain and skeletal muscles
how is creatine phosphate used
process called substrate phosphylation where ATP is made
how is creatine used by athletes
could create greater energy reserves but the muscle has limits creatine storage
uses are unknown so far
howis glycogen used by musce=les
broken down into a form of glucose without any oxygen required
how do muscles get oxygen
blood
or stored in myoglobin
what is mypglobin
protein found in muscles for oxygen and iron binding
Myoglobin increases the solubility of oxygen.
Myoglobin facilitates oxygen diffusion
what does high pH do to haemoaglobin
low H+
promotes tigher binding of oxgen
curve to left
whatdt does low pH do to haemoaglobin?
higher H+
permites easier release of oxygen
curve to right
what happens to lactic acid?
absorbed by theliver
converted into pyruvate ad glucose
how is oxygen used in revocery afte exercise
replenish oxymoyglobin
metabolise fatty acids in the krebs cycle to make energy
how is energy used in recover after exercise
restore levelss of phospcreatine
syntehsiese glycogen from absorved glucose
red muscle
oxidative
white muscle
glycolytic
features of oxidative red muscle
small high mitochondra ATP made slow contractions red due to high myoglobin
what type of contraction do red muscle have
ssustained every and can maintain contraction for long times
contractio is slower
where are red muscles found?
postural muscles
features of white glycolytic muscle
bigger muscles
low mitochondrai
less dense and light colour
uses glycogen rather than moyglobin
how do white glycoloytic muscle contract
hugh amount of power
but easily fatigued
types of rd muscle
fast and slow twitch oxidative muscles
what is myosin isoform I
slow twitch oxidative red muscle
what is moysin isoform type IIA
fast twitch oxidative glycolytic red muscle
what is myosin isoform IIB
fast twitch glycolitic white muscle
whats the difference between slow twitch oxidative red muscle and fast twitch oxidative glycolyitic red msucle
slow is oxidative and aerobic
fast oxidative glyolytic is glycolytic but becomes more oxidative with endurance training
